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FRACP > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the clinical features of PRES (posterior reversible encephalopathy syndrome)? Aetiologies? Which other name does it go by?

A

Features: headache, confusion, seizures and visual loss

Aetiology: malignant HTN, pre-eclampsia

AKA: Reversible posterior leucoencephalopathy

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2
Q

Give causes of small pupils.

A

Causes of SMALL pupil (AHA-POO)

Argyll-Robertson pupil (neurosyphilis / DM)
Horner’s syndrome
Age
Pontine CVA
Opioids
Organophosphates
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3
Q

Give causes for dilated pupils.

A

Causes for dilated pupils
“CHEAT and you die!”

Carbon monoxide - SUICIDE
Holmes-Adie pupil – post-infective damage to post-ganglionic ANS/PSNS
Ethylene glycol - SUICIDE
Atropine
Third nerve palsy
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4
Q

What is Miller-Fisher syndrome? How is it diagnosed (triad and blood test)?

A

Miller Fisher syndrome:

  1. Variant of GBS
  2. Post-infective triad (AOA): areflexia, ophthalmoplegia, ataxia
  3. Ix: GQib (ganglioside IgG Ab) – 95% specific
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5
Q

What are anti-purkinje Abs?

A

Anti-pukinje cell Abs detect

  1. subacute cerebellar degeneration
  2. autoimmune peripheral neuropathy from breast/gynae carcinoma
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6
Q

What is Refsum’s disease? How is it treated?

A

Genetic cause of demyelination.

Autosomal recessive disorder that leads to phytanic acid oxidase deficiency causing a build-up of phytanic acid and demyelinating polyneuropathy.

Rx: phytanic acid restricted diet - avoid fats from animals/fish.

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7
Q

What is Lewis-Sumner syndrome?

A

Asymmetric variant of CIDP (chronic inflammatory demyelinating polyneuropathy).

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8
Q

Give 7 causes of demyelinating polyneuropathy.

A

Immunology-related (3):
Guillain-Barre Syndrome
CIDP (or Lewis-Sumner if asymmetric)
HIV

Genetic (2):
Hereditary motor sensory neuropathy
Refsum’s disease

Drug (1): Amiodarone

Cancer (1): Paraproteinaemia

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9
Q

Give 4 causes of axonal polyneuropathy.

A 
DAVV:
DM
Alcohol
Vasculitis
Vitamin deficiency
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10
Q

Regarding nystagmus, which phase (slow vs. fast) defines the direction of the nystagmus?

A

Fast phase.

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11
Q

What are the 4 main causes of nystagmus (consider anatomy)?

A
  1. Visual disturbance
  2. Labyrinth lesion
  3. Vestibular lesion
  4. Brainstem/cerebellar lesion
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12
Q

What is anisocoria?

A

Unequal pupils. Normal in 20% of population but may reflect a benign or serious condition.

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13
Q

In a case of anisocoria, how does one determine which pupil is abnormal?

A

The abnormal pupil can be identified by examination in light and dark conditions.

Anisocoria that is greater in the DARK identifies the SMALL pupil as abnormal and implies a lesion in the SYMPATHETIC pathways e.g. Horner’s syndrome (AHA-POO causes of small pupil)

Anisocoria that is more pronounced in LIGHT conditions identifies the LARGE pupil as abnormal and implies a lesion in the PARASYMPATHETIC pathways e.g. Holmes-Adie pupil (CHEAT causes of dilated pupil)

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14
Q

True/False: Marcus-Gunn pupil causes anisocoria.

A

False.

Marcus-Gunn pupil is NOT associated with unequal pupils

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15
Q

What is a Marcus-Gunn pupil and what is it usually due to?

A

Relative afferent pupillary defect suggest lesion to optic nerve or retina (i.e. afferent pupillary pathway). Abnormal eye paradoxically dilates to light exposure.

Lesion in optic nerve is between retina and optic chiasm.

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16
Q

Describe the 2 neurotransmitters of the autonomic nervous system (ANS = SNS / PSNS).

A

Ach: secreted by all neurons of the ANS, except the post-ganglionic neurons of SNS.

Norad (and some Adr): secreted by post-ganglionic neurons of SNS.

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17
Q

What are the 3 main sites that catecholamines are produced in the body?

A
  1. Post-ganglionic neurons of SNS
  2. CNS
  3. Adrenal medulla (chromaffin cells)
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18
Q

What autonomic system structure is the adrenal medulla analogous to?

Why does it produce more adrenalin than noradrenalin?

A

Adrenal medulla = post-ganglionic neuron of SNS.

Glucocorticoids from the adrenal cortex promotes increased levels of PNMT (phenylethanolamine-N-methyl transferase) which converts noradrenalin to adrenalin.

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19
Q

What spinal lesion would cause weakness of finger flexion?

A

Spinal lesion at level C8

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20
Q

Brachioradialis (supinator reflex) is mediated by which spinal level?

A

C5/C6

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21
Q

I was told a fantastic mnemonic for REFLEXES that went like ‘1,2,3,4,5,6,7,8’

WTF?

A

From inferior to superior:

1,2,
3,4,
5,6,
7,8

S1,S2 = ankle jerk
L3, L4 = knee jerk
C5, C6 = biceps
C7, C8 = triceps

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22
Q

I was told another awesome mnemonic for REFLEXES that went like ‘1-2 buckle my shoe, 3-4 kick the door, 5-6 pick-up sticks, 7-8 lay them straight’

A

S1,S2 = ankle jerk (shoe = ‘s’)

L3, L4 = knee jerk

C5, C6 = biceps

C7, C8 = triceps

23
Q

Mnemonic for upper limb peripheral nerve palsies?

A

DR CUMA:

Dropped wrist
Radial nerve palsy

Claw hand or ‘hand of benediction’ (flexion of 4th + 5th digit)
Ulnar nerve palsy

Median nervel palsy
Ape hand - loss of thumb abduction

24
Q

The ‘OK’ sign with the hand test motor function of all three nerves of the hand, how?

A

Radial nerve palsy = inability to dorsiflex the hand (wrist drop)

Ulnar nerve: inability to abduct 4th and 5th ulnar digits (claw hand)

Median nerve palsy = inability to abduct thumb (ape hand)

25
Q

True/False: brief episode of neurological deficit that last < 24 associated with brain injury on imaging is considered a TIA.

A

False: not according to the new definition of TIA.

26
Q

True/False: stroke is often associated with LOC and/or confusion.

A

False.

Stroke mimics are suggested if:

  1. known cognitive impairment
  2. LOC/seizure at onset
  3. Patient able to walk with no lateralising symptoms
  4. Confusion and NO neurological symptoms
27
Q

Which of the following interventions for ICH has evidence to suggest benefit:

  • Surgery / clot evacuation
  • Lower BP to < 140/90
  • Transexamic acid
  • Stroke unit
A

Only stroke units yield demonstrable benefit

28
Q

For a large hemispheric stroke, grade the following in terms of greatest RRR to least:

  • Stroke unit
  • tPA
  • Hemicraniectomy
  • Aspirin
A

Greatest RRR

Hemicraniectomy
tPA
Stroke unit
Aspirin

Least RRR

NB: patient may survive hemicraniectomy but QoL may be poor!

29
Q

What are the cascade of neurological deficits associated with B12 deficiency?

A

Peripheral neuropathy THEN
Loss of vibration and position sense THEN
Areflexia and weakness THEN
Spasticity with extensor babinskis +/- ataxia

30
Q

What is Neuralgic Amyotrophy?

A

Upper plexopathy that is usually post-infective.

Initially with days to weeks of pain then weakness and sensory loss correlating to C5-7 territory.

Self limiting condition (may take years).

31
Q

What is the triad for normal pressure hydrocephalus?

A

3Ws (wet, wobbly and wacky):

  1. Urinary incontinence
  2. Ataxia
  3. Confusion / memory impairment
32
Q

What is Syringomyelia?

A

Fluid filled cavity (syrinx) in the spinal cord (often cervical spine - C2-C9) that elongates and enlarges causing compression of:

  • Corticospinal tract (ipsilateral motor)
  • Spinothalamic tract (contralateral pain and temperature)
  • Anterior horn cells
33
Q

What are the clinical features of Syringomyelia?

A

Headaches

Motor deficit (CsT): ascending weakness/wastig of 
hands then forearms then shoulders

Bladder symptoms

Absent reflexes

Central cord deficit (sensory loss in pain and temperature (StT), then light tough and propioception)

34
Q

What is Syringobulbia?

What is it often associated with?

What population is it more common in?

A

Synrinx extends into brainstem that is often associated with a Chiari malformation that impairs CSF circulation.

More common in men in 20-30s.

35
Q

How is syringomyelia or synringobulbia treated?

What investigation should NOT be done?

A

Early surgical decompression with shunt insertion.

Do NOT do a lumbar puncture.

36
Q

What clinical features distinguish an L5 radiculopathy from a common peroneal nerve lesion (4)?

A

L5 innervates everything the common peroneal nerve does PLUS tibialis posterior + gluteal muscles.

‘Knowing this makes you to look FLASH! (L for L5)

Foot inversion lost
Ankle reflex lost
Sensory loss (dorsum of foot and lateral leg)
Hip abduction and internal rotation lost

37
Q

Match the following epic list of antibodies to their conditions:

Anti-NMO
Anti-GQ1b
Anti-GM1
Anti-MAG
Anti-ACh receptor
Anti-MuSK
A

Anti-NMO = Devic’s disease
Remember: Anti-NEMO… you must be a DEVIL!

Anti-GQ1b = Miller Fischer
Remember: Dr Fischer does not like GQ magazine!

Anti-GM1 = Multifocal Motor Meuropathy (MMN)
Remember: Good Morning grandpa! Time to put on your MULTIFOCAL glasses to start the day.

Anti-MAG = Waldenstroms or Distal Acquired Demyelinating Symmetric (DADS) Polyneuropathy (distal sensory loss)
Remember: Cool MAGS are for DADS that are not WALLflowers!

Anti-ACh receptor = Myasthenia Gravis (MG)

Anti-MuSK = MG with respiratory distress and bulbar involvement (less eye involvement)
Remember: This MUSKy smell burns my throat and lungs!

38
Q

What is the presentation of Multifocal Motor Neuropathy (MMN)?

How is it treated?

A

MMN present with LMN deficit arm > legs

Responds to steroids and IVIG.

39
Q

What condition is Devic’s disease similar to?

How do they present?

A

Similar to multiple sclerosis

Except there are NO oligoclonal bands in the CSF, with predominance of PMN in CSF.

Presents with vomiting and painful optic neuritis.

40
Q

Patient presents with Anti-MAG in blood and distal sensory loss. Diagnosis?

A

Distal Acquired Demyelinating Symmetric (DADS) Polyneuropathy

41
Q

Patient presents with symptoms similar to Myasthenia Gravis with sparing of the eyes and SOB. Bloods reveal Anti-MUsK antibodies. Diagnosis?

A

Seronegative MG

42
Q

What is Lamber-Eaton myasthenic syndrome (LEMS)?

A

Rare autoimmune disorder characterised by weakness in the limbs due to Abs to presynaptic voltage-gated calcium channels

Often associated with malignancy (e.g. SCLC) and is considered a paraneoplastic syndrome.

43
Q

What part of the brain is implicated with a SEMANTIC memory deficit?

How might you test this?

A

Test: ask patient to differentiate different animals.

Left (DOMINANT) lateral temporal lobe.

44
Q

What are the clinical features of a frontal lobe lesion?

A

Perseveration

and

REDUCED:
attention / memory
calculation / planning
activity / spontaneous activity
concern (loss on inhibition)
45
Q

Patient presents with a ‘pure’ sensory or motor stroke, where is the lesion?

What is the prognosis?

A

Lacunar stroke - discrete lesion in the contralateral PONS or INTERNAL CAPSULE.

Good prognosis

46
Q

Patient present with dysarthria and clumsy hand syndrome, where is the lesion?

A

Contralateral pons.

47
Q

Name 6 drugs that may cause DEMYELINATING neuropathy.

A

PPATTC (Patsy!)

Procainamide
Perhexeline
Amiodarone
TNFi
Tacrolimus
Chloroquine
48
Q

Name 3 drugs that cause AXONAL neuropathy,

A

VET:

Vinca-alkaloids
EtOH
Thalidomide

49
Q

What is Gerstmann syndrome?

A

Stroke of the dominant parietal lobe:

  1. Alexia (cannot write)
  2. Acalculia
  3. Finger agnosia
  4. Right-left disorientation
50
Q

What is the consequence of a stroke to PICA?

A

Lateral Medullary Syndrome / Wallenberg:

  • ipsilateral loss of pain and temp in face
  • contralateral loss of pain and temp in body
  • Vertigo / dysphagia / dizziness / ataxia / nystagmus
51
Q

What is Weber’s syndrome?

A

PCA lesion:

  • Ipsilateral CNIII lesion
  • Contralateral weakness
52
Q

What are the CNs that subserve the corneal reflex?

A

Sensation (afferent) = CNV

Motor (efferent) = CNVII

53
Q

What are the characteristic findings of motor neuron disease?

A

LMN deficit in upper limbs and UMN deficit in the lower limbs.

UMN (everything goes up): reflexes, tone, plantars

LMN (down): refelexes, tone, plantars

54
Q

What are the side effects of phenytoin (mnemonic = PHENYTOIN)

A

PHENYTOIN:

P: P-450 interactions
H: Hirsutism
E: Enlarged gums
N: Nystagmus
Y: Yellow-browning of skin
T: Teratogenicity
O: Osteomalacia
I: Interference with folic acid absorption (hence anemia)
N: Neuropathies: vertigo, ataxia, headache

FRACP (20 decks)

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